The estimated 5-year overall survival among the group of men who had delayed ADT was 87.2% compared with 85.1% for those who had immediate ADT following a PSA-based relapse. Ten-year survival was 71.6% for both groups.
The prostate cancer-specific mortality was also similar for the two groups: the 5-year survival for the immediate and delayed ADT groups was 96% and 93.3%, respectively, and the 10-year survival was 90.2% and 89.4%, respectively. All of the patients were previously treated with radical prostatectomy or radiotherapy.
These results, based on an analysis of 2,022 patients that are part of the national prospective registry CaPSURE (Cancer of the Prostate Strategic Urologic Research Endeavor), were presented by study author Xabier Garcia-De-Albeniz, MD, of the department of epidemiology at Harvard School of Public Health, at a press briefing in advance of the 2014 American Society of Clinical Oncology (ASCO) Annual Meeting, which will take place May 30–June 3 in Chicago.
“The role of starting ADT in these patients is not clear,” said Garcia-De-Albeniz during his presentation at the press briefing. Garcia-De-Albeniz referred to the National Comprehensive Cancer Network guideline, which states that there is “a therapeutic dilemma” regarding the role of ADT. Additionally, the potential magnitude of the benefit, particularly for asymptomatic patients, needs to be understood, according to ASCO guidelines.

Joe:
Very interesting study. Over the years I have subscribed to Dr. Myers thinking on this issue; he set forth his position as described in one of my journal entries awhile back:

Since releasing my last journal entry, which in retrospect appears a tad panicky, I discovered in my ever-growing stockpile of prostate cancer materials an article written by Dr Charles (Snuffy) Myers that reduces my concern. In a discussion relating to a rising PSA following prostetectomy Dr Myers points out some patients will not experience serious health problems until PSA values reach between 1000 and 2000. He goes on to explain that a person with a doubling time of one year and a PSA of 3.96 like myself will not reach the danger zone for about eight years. To think it may be possible to continue my current quality of life without seriously jeopordizing my general health for this period of time is very, very comforting. My gosh, why has none of the experienced clinicians that I have interacted with since my PSA began to rise called this medical data to my attention? Phenomenal! Unbelievable! With that said let me provide a little counterpoint as did Dr Myers. Just as I recently hedged my bet (refer to my previous journal entry), Dr Myers engages in a little scientific hedging of his own. Immediately following his statement about the absence of serious health problems until one's PSA exceeds the 1000 mark, he goes on to say "Despite this I begin treating my patients as soon as the PSA begins to raise".

He supports this practise by citing a number of studies that suggest by doing so longterm outcomes are improved.

My case manager responded to my UFPTI inquiry as follows (paraphrased): "Your PSA remains low: "Our advice for you is to stay the course, i. e., continue to watch and wait". So where does this new infomation leave me? Emotionally I feel less panic stricken. Intellectually I still feel the need to locate a knowledgable prostate cancer specialist to serve as a sounding board and technical advisor. I intend to pursue this goal , perhaps at a more leisurely, less frantic pace. An observation: The roller coaster ride is no less tumultuous than when I commenced this excursion several years ago. As they tend to say these days: I can't make this stuff up "

In any event these two studies illustrate an extremely troublesome aspect of PCa, that is, not even the acknowledged experts agree with one another. The best that we PCa warriors can do is to research our options to the best of our abilities, place our bets and hope for the best. Its a crapshoot and has been for far too long.

A final thought: science indicates testosterone nourishes PCa. Logic suggests it may be beneficial to reduce or block its production.

Monday, July 31, 2017

An extremely frustrating aspect of a PCa diagnosis has been the lack of consensus among the recognized experts. Most all practitioners including urologists, radiologists (a diverse group unto themselves), medical oncologists and a variety of surgeons appear to regard us as an ideal candidate for their area of expertise. Too often we PCa warriors rely on the first specialist we encounter or equally worrisome we research our options to the best of our ability and base our decision on woefully incomplete data. Either way it's a crap shoot. For the life of me (said with tongue only partly in cheek), I can think of no other affliction where the treatment choice is so problematic.

A couple of months ago the TV program "Sixty Minutes" covered a potential solution to our dilemma. The show featured a cancer center located at the University of North Carolina where a team of experts develop treatment plans for cancer patients who have failed standard therapy using the computerized Watson System of Artificial Intelligence. AI capability enables the team to formulate more effective plans based on all the medical literature published world wide including up-to-date clinical trial data.

Wouldn't it be nice if one institute or another with Watson AI capability focused on prostate cancer? Us PCa warriors can only hope.

Thursday, April 20, 2017

Over the past year my PSA has risen slowly but surely from .11 to .76. As any reader of this journal knows, I searched long and hard for a solution with a high likelihood of success with minimal side effects. Rightly or wrongly throughout my ordeal I have placed a premium on preserving quality of life. To my way of thinking a cure would be most welcome, but the risk involved has inevitably tended to over shadow the desired outcome. Its been a crapshoot from the outset and that has never changed.

At this juncture I am pleased to report that after being on xtandi for only three weeks my PSA has dropped back to .11.The predominant side effect of fatigue has materialized as expected. In my case this means after two hours of tennis doubles three days a week I tend to fall asleep in the evenings while attempting to catch up on my reading or watching a sporting event on TV. Short story abbreviated to the max, I am satisfied with my results thus far. A brief but pertinent Patient Portal exchange with Dr. Myers appears below:

Pt.

Assuming xtandi proves effective as indicated by my monthly blood draws, how long do you expect this medication to control the progression of my PCa?

Sunday, March 12, 2017

"As per your request, I consulted with a specialist at Univ. of Mich. who performs all of the hospital's prostate cryosugeries. He advised me that his outcomes parallel the national norms as outlined below:

In a subsequent exchange of emails, a patient of yours and a friend of mine, informed me that he has been on xtandi for nine months. He expressed complete satisfaction with his results to date. His only side effect is fatigue which he counteracts with a daily nap.

At one point you were prepared to put me on xtandi, but decided otherwise based on the fatigue factor. Although xtandi may not offer the prospect of a cure as does cryosurgery my personal preference would be to initiate what you at one time labeled Hormone Lite (Xtandi). Can we reconsider this option?"

Friday, January 27, 2017

I have devoted considerable time and effort attempting to identify a safe and effective means to control or eliminate my recurrent PCa. I outlined the history of this endeavor in my previous journal entry. I have tentatively decided on the following ADT protocol recommended by a medical oncologist I consulted at the University of Michigan : Intermittent three-month-duration Lupron injections to be administered each time my PSA rises to 7.0. My current PSA is .60. His educated guess is it will take two years before the first injection will be needed. In the meantime, as per his recommendation, I will continue on Casodex as prescribed by Dr. Myers.

Up to this point I have avoided Lupron like the veritable plague. I first learned of ADT researching options following my diagnosis in 2008. The known side effects are "off-putting" to say the least. It's a bit difficult to fathom at this point, but Lupron appears to be my best choice. For more perspective in this regard I have included a rough draft of a journal entry that I chose not to use until now: see below:

"ADT with Lupron is a form of medical castration. It is designed to do many of the same things as surgical castration (orchiectomy). It is associated with a range of side effects that many men find to be highly delibitating and emotionally devastating, including loss of libido, loss of sexual function, genital shrinkage, hot flashes, weight gain, loss of bone mass, "Lupron Brain"(difficulty in concentrating, clarity of thought, memory loss, etc.) enlargement of the breasts and other symptoms of gynecomastia, and a long list of less common problems. This is not a form of therapy I would wish on anyone if it could be avoided. ADT on its own is not curative and has never been established to extend the survival of men with advanced prostate cancer. It is a palliative form of care whose primary function is to minimize the risk of bone pain associated with advanced prostate cancer. Many clinicians believe that all too many men with progressive prostate cancer are treated much too early with ADT because it can be used to manage the patient's PSA level. However overly early use of ADT is also associated with risk for early onset of castration-resistant prostate cancer. ADT has shown to have a survival benefit only when used in combination with external beam radiation therapy for men with locally advanced prostate cancer (and to have a curative impact in some of these patients)."

2012 PSA rose from .8 to 2.59 from May to Oct.; Dr. Kwon of Mayo Clinic identified a small cancerous lesion in prostate by Choline Scan. Mayo Clinic reviewed my biopsy slide and determined my Gleason to be 4+4

2013 Began Hormone Lite as prescribed by Dr. Charles Myers; see below:

I. Prescription Drugs

A. Metformin 500 MG 2 daily. Anti-cancer

B. Avodart .5 MG 3 a week. Anti-cancer

C. Casodex 50 MG 3 weekly. Anti-cancer

D. Zocor 10 MG 1 daily. Anti-cancer

E. Losartan 50 MG 1 daily. Blood pressure.

II. Supplements

A. Pomegranate 1 daily 10 MG. Anti-cancer

B. Vitamin B12 1000mcg

C. Vitamin D3 5000 IU 2 daily. Restore deficiency

D. Super Bio-Curcumin 400 MG 1 daily. Anti-inflammatory

E. Optmized Resveratol 250 MG 1 daily. Anti-inflammatory

III. Mediterranean Diet

2015

I.PSAs rose from .077 in Jan. to .18 in Aug. Dr. Myers increased my Casodex from three times weekly to a daily dosage. PSAs returned to their former lower levels.

II. Endorectal MRI at VCU; 3x5 mm tumor identified

2016 PSAs ascend from .11 in Apr to .49 in Dec. Follow-up endorectal MRI at VCU; tumor more than doubled in size to 10x7 mm .

I have considered several options the past few weeks including Pencil beam PBRT, cyberknife, prostatectomy, brachytherapy, focal beam ablation, cryotherapy , Hi Fu, modified hormone lite, full blown hormone therapy and chemotherapy. The first seven options have been pretty much eliminated each for a different reason. More recently an advisor recommended estrogen therapy which looks promising at least for a temporary period (a year or so?)

Major changes under consideration; too early and too fluid to document.

Monday, October 31, 2016

Over the past few months my PSA has risen incrementally as shown below:

April .11

May .18

June .24

July .29

Aug. .38

Sept. .38

Oct. .39

In response to these numbers Dr. Myers and I discussed several options via the Patient Portal including radiation, surgery, full blown hormonal therapy (I. e., complete suppression of testosterone along with its concomitant adverse side effects) and modification of Hormone Lite by substituting xtandi for casodex. We agreed on the latter, but decided to postpone action to monitor my PSAs awhile longer.

I pondered this discussion over the next few days and returned to the Patient Portal to raise a few related concerns. I advised Dr. Myers it would give me peace of mind if I knew whether he had guidelines in mind as to when action may be indicated. More specifically I posed the following questions: (1) Will we wait until my PSA reaches a certain level? (2) If so what might that number be? (3) Is the speed of ascension a determinate? As was his prerogative Dr. Myers chose not to respond. Rather than press him for answers via the internet, I elected to revisit these concerns at our upcoming annual appointment which occurred a few weeks later on October 26.

The planned informational exchange did not occur. Au contraire! I got blindsided and bushwhacked. The meeting began as usual. Initially a medical technician conducted a few routine tests, e. g., blood pressure, weight, temperature etc. Dr. Myers' physician's assistant continued with a few routine preliminaries. Out of the blue she dropped the following bombshell: "It would appear the casodex has ceased to control the progression of your PCa. It is also conceivable that the casodex has begun to nourish the cancer. She continued with the following barrage: "You might wish to consider Cyberknife intervention. There is a physician in California who has demonstrated considerable success with this technique." Her frontal attacks were subsequently supported by Dr. Myers who added the option of PBRT. While xtandi and full blown hormone therapy should remain in the mix, Dr. Myers wanted me to understand, both of these options harbored the risk of castration resistance resulting in a painfully slow, agonizing death. In any event before deciding on a course of action Dr. Myers and his PA agreed a follow up endorectal MRI was an essential prerequisite. Dr. Myers urged me to have this procedure performed by VCU in Richmond Virginia since it was this clinic who provided the "benchmark" examination two years ago.

So there you have it. The tumultuous journey is back on track with a vengeance. The endorectal MRI is scheduled for November 12th at VCU. Stay tuned.